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Karim A. Alavi, M.D.1


Amebiasis is an important cause of death from parasitic disease worldwide. The

causative organism is Entamoeba histolytica, which has an infective cyst stage and a
pathogenic and motile trophozoite stage. The clinical presentation can vary from an
asymptomatic carrier state to fulminant colitis and colonic perforation. The majority of
patients can be managed medically. However, a small percentage of patients require urgent
exploration and resection with an associated high mortality rate. Early recognition and
initiation of medical therapy including treatment of asymptomatic carriers are vital to
preventing catastrophic outcomes.
KEYWORDS: Ameba, colitis, fulminant, parasite

Objectives: On completion of this article, the reader should be able to summarize the diagnosis and management of intestinal

ntestinal infestation with Entamoeba histolytica

is common throughout the tropics and subtropics, where
it is endemic. It is the second leading cause of death from
parasitic disease worldwide. In the United States, amebiasis has become the most frequent parasitic infestation
encountered by surgeons. This is largely due to the
migratory inux of immigrants from Mexico and Central America, where amebiasis is endemic.1Conversely,
there is a reported incidence of 20% to 30% in selected
populations of homosexual men in North America and
Europe.2 Despite its growing incidence, there is limited
mention of amebiasis and acute fulminant amebic colitis
in major surgical textbooks dealing with diseases of the
colon and rectum. Amebic colitis can often arise in a
similar fashion to other colitides, but failure of the
treating physician to consider this in the differential
may lead to catastrophic complications. The purpose of
this article is to review the pathogenesis, clinical presentation, work-up, and management of amebiasis.

E. histolytica exists in two forms: a nonmotile cyst, which
is infective, and a motile trophozoite stage, which causes
the invasive disease. The trophozoite lives in the wall
and lumen of the colon.3 Often the cytoplasm of the
trophozoites contains ingested red blood cells, which
aids in the diagnosis.4 Trophozoites, however, do not
exist outside the body and therefore do not transmit the
disease. The primary mode of transmission is ingestion
of cysts from contaminated food or water. Venereal
transmission also occurs through the fecal-oral route.
Once ingested, the cyst disintegrates in the small bowel
and releases the trophozoites in the colon. These organisms live in the colon and feed on the bacteria and
supercial mucosal cells, occasionally invading deeper
and resulting in distant disease. The parasite creates a
mucosal defect and a characteristic ask-shaped ulcer
with necrosis in the submucosa and muscularis of the

Division of Colon and Rectal Surgery, Department of Surgery,
University of Minnesota, St. Paul Minnesota.
Address for correspondence and reprint requests: Karim A.
Alavi, M.D., Division of Colon and Rectal Surgery, Department of
Surgery, University of Minnesota, 393 Dunlap Ave. North, Ste. 500,
St. Paul, MN 55104. E-mail: alav0006@umn.edu.

Miscellaneous Colitides; Guest Editor, Judith L. Trudel, M.D.

Clin Colon Rectal Surg 2007;20:3337. Copyright # 2007 by
Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY
10001, USA. Tel: +1(212) 584-4662.
DOI 10.1055/s-2007-970198. ISSN 1531-0043.




The inammatory response can be slight with

intervening normal mucosa, or at times the tissue can
be indistinguishable from that in ulcerative colitis, even
progressing to frank perforation. Transmural necrosis
has been shown to be due to amebic invasion of the
segmental arteries of the colon, with consequent thrombotic occlusion and necrosis.6 The omentum plays a role
in sealing the perforations and is believed to aid in
revascularization of the colon. Lesions can occur anywhere in the colon but appear more frequently in the
cecum and ascending colon and less frequently in the
rectum and sigmoid. Occasionally, the trophozoite enters the portal circulation and travels to the liver, creating
an amebic liver abscess.7,8 Rarely, they travel to the brain,
resulting in abscesses,9 and to the perineum, genitalia,
and skin, creating ulcerations.10
E. histolytica is distributed throughout the world and
poses a signicant health risk in locations where barriers
between feces and food and water supplies are limited.
Entamoeba exists as two genetically distant species
Entamoeba dispar, a commensal, and E. histolytica, the
pathogen. This has changed our understanding of the
prevalence and distribution of the parasite worldwide.
Indeed, the majority of the asymptomatic individuals
infected are actually colonized with E. dispar, an organism that is not a pathogen and causes no mucosal
disease even in severely immunocompromised individuals.11E. histolytica has also been demonstrated in stool
samples of asymptomatic patients, yet it is also the
causative agent in amebic colitis and associated extraintestinal manifestations. Amebiasis can spread within
families; therefore, household contacts of patients with
the disease should be screened for colonization and
Approximately 40,000 to 100,000 people die
yearly from amebiasis, making it the second leading
cause of death from parasitic diseases.5 In the United
States, the majority of the reported cases are in immigrants from or travelers to endemic areas such as
Mexico, Central America, and South America. A subgroup of the population that needs to be addressed is
homosexual men. A prevalence rate of 20% to 30% has
been documented in selected populations of homosexuals of North America and Europe.12 A study of a
venereal disease clinic population demonstrated 55%
positivity rate for E. histolytica from repeated stool
specimens, although there was only 56% compliance.13
The relationship is thought to be related to a large
reservoir of infection and a prevalent mode of transmission, such as oral-anal sex, promiscuity, and anal
hygiene. Despite the frequent isolation of E. histolytica
from homosexuals, the occurrence of amebic colitis or
liver abscesses is infrequent.


Amebic colitis affects children and adults of

both sexes equally. However, amebic liver abscesses
appear more often in men between the ages of 18 and
50, in whom rates are 3 to 20 times higher than in
other populations.14 The reason for this profound
difference is unknown. Several studies have suggested
that hormonal differences between sexes may play a
vital role.7
Amebic disease has a variety of clinical manifestations.
These can be subdivided into intestinal and extraintestinal presentations. Within any one patient there can be
considerable overlap in the sites of infection.
The majority of patients are asymptomatic carriers. The
organism lives in the bowel lumen and sheds cysts in the
stool. The potential for invasion still exists in these
patients, and it seems reasonable to begin these patients
on treatment. Indeed, 4% to 10% of asymptomatic
carriers eventually develop invasive disease.15
Clinical presentation can vary from fulminant
colitis to mild, intermittent episodes of blood-tinged
diarrhea. Associated symptoms include fever (< 40% of
patients), weight loss, dehydration, and anorexia. Symptoms can persist for months to years with asymptomatic
intervals.16,17 Others have signs and symptoms similar to
those of ulcerative colitis, with a small percentage
developing toxic megacolon.18 The lack of specicity
means that amebiasis must be considered in the differential diagnosis for all patients presenting with colonic
Physical ndings vary from no ndings to mild
tenderness with an enlarged liver. Occasionally, patients
present severely ill with tachycardia, hypotension, and
peritonitis.15In this group, perforation must be considered and quick action is necessary as mortality is high.
Routine blood counts vary from normal to mild anemia.
However, severe anemia is rare.15
Noncolitic diseases, such as amebomas and strictures, are infrequent. Strictures can be long or short,
symptomatic or asymptomatic.17 They can mimic malignancy, mandating biopsy. Amebomas appear as tumorsrm and nodular, with a brous outer wall and an
inner core of necrotic tissue and trophozoites. They
occur most frequently in the cecum and appear as lling
defects on barium enema.17Amebomas can occur in the
presence of active colitis or can be independent of active
disease, mimicking malignancy. The differentiation is
important as the treatment for an ameboma is medical.
They often disappear after initiation of appropriate
therapy.15On examination, a right lower quadrant mass
or a rectal mass may be palpated.



The most common extraintestinal manifestation of the

disease is amebic liver abscess. The disease usually
predominates in young adult males. It usually arises
from spread by the portal circulation as amebic trophozoites breach the colonic mucosa. In the liver they
produce a well-circumscribed area of necrosis surrounded by a halo of hemorrhagic tissue, which eventually progresses to a cavity containing necrotic
debris.8Characteristically, the uid is chocolate brown
or resembles ketchup and is usually odorless and sterile.
The trophozoites are most often found in the wall of the
Microscopic examination of the stool is often
negative for E. histolytica trophozoites or cysts.7 A careful history is mandatory as individuals can present
months to years after travel to endemic regions. The
most common presenting symptom is right upper quadrant pain with radiation to the shoulder, right chest, or
epigastrium, often accompanied by fever, night sweats,
malaise, and anorexia. Additional signs can include a
nonproductive cough and anorexia. On physical examination the patient often appears tired, wasted, febrile,
and uncomfortable. There may be rales over the right
lung base and a tender, enlarged liver. Patients often
have a leukocytosis, mild anemia, elevated alkaline
phosphatase, and an elevated erythrocyte sedimentation
rate. The presentation can often be acute, less than
10 days in duration, or it can be chronic with anorexia
and weight loss. The colon is rarely involved, so endoscopic examination is of minimal value. Computed
tomography is a helpful adjunct in making the diagnosis.
In one series of amebic liver abscesses, 83% of the lesions
were located in the right hepatic lobe.20 Finally, indirect
hemagglutination assay, which detects antibodies directed against Entamoeba, is a critical laboratory test
and is positive in 100% of patients with amebic invasion.
Early false-negative results do occur, so the test should
be repeated if clinical suspicion is high.21
Amebic liver abscesses can extend into the thorax,
producing an empyema (7% to 20% of patients),22,23 or
into the pericardium.23 They can freely rupture into the
peritoneum (2% to 7% of patients)24 and bowel. Overall,
mortality rates are low with thoracic involvement
patients present with a productive cough and sputum
containing trophozoitesbut increase with pericardial
(mortality rate of 30%) and peritoneal involvement.2224
This further substantiates the role of an early treatment

Amebic brain abscesses are rare and arise concurrently

with hepatic abscesses (0.1% of hepatic abscess cases),
demonstrating the importance of invasion in their

pathogenesis.9 Patients present with sudden onset of

symptomsheadache, seizures, vomiting, and mental
status changes, with a rapid progression to death. Outcomes appear to improve with early initiation of medical

There have been case reports of urinary tract problems,

rectovaginal stulas, perianal disease, and cutaneous
The diagnosis of amebic colitis depends on the demonstration of Entamoeba in the stool or the colonic mucosa
of patients. A single formed stool will demonstrate one
third to half of amebic infections, and examining three
successive stools on three separate days improves the
yield to 60% to 70% of patients with colitis and 43% of
patients with amebic liver abscesses. Furthermore, barium, bismuth enemas and antibiotics can interfere with
the study, producing false-negative results.26 However,
this method cannot distinguish between E. histolytica
and its nonpathogenic counterpart E. dispar.
With escalating health care costs, it is difcult to
justify keeping patients under observation without initiating medical therapy. As a result, serologic testing has
become a valuable adjunct in the diagnosis of amebiasis.
Numerous tests are available, but the indirect hemagglutination assay (IHA) is highly sensitive with a high
negative predictive value. In one study, 91% of patients
with amebic colitis and 95% of patients with amebic liver
abscesses had a positive IHA A negative test implies that
invasion did not occur.27 IHA remains positive for up to
20 years and does not differentiate a previous infection
from an acute one. However, this test is expensive,
require experience to perform, and requires time to
demonstrate results.
Endoscopy can be a useful adjunct in the diagnosis. Ulcers can grow to approximately an inch and have
a ask shape. They are often covered with a yellow
exudate. The intervening mucosa is often normal in
appearance. Fulminant colitis can have an endoscopic
appearance similar to that of diffuse ulcerative colitis,
underlining the importance of a thorough clinical
The cornerstone of treatment for amebiasis remains the
nitroimidazole derivatives (metronidazole, tinidazole,
ornidazole). Ninety percent of patients are cured with
metronidazole at 750 mg three times per day.3 Surprisingly, resistance has not been detected. Following a




10-day course, treatment with a second-line intraluminal

agent (paromomycin, iodoquinol, diloxanide furoate) is
required to eradicate the colonization. Follow-up stool
examination is recommended in all patients to ensure
clearance. Asymptomatic carriers with documented E.
histolytica should be treated with a luminal agent to
eradicate the infection.28,29 This is based on the known
risk of developing invasive disease in these patients. In
addition, these individuals shed cysts and are a potential
risk to public health. Interestingly, E. dispar infection
does not require treatment but is a marker for exposure
to contaminated food or water, or both.
The majority of patients respond well to medical
management alone. Occasionally, for unknown reasons,
the disease progresses to a fulminant necrotizing colitis
that may be indistinguishable from other forms of acute
colitis. This is a rare but frequently fatal complication. It
is vital to recognize the difference early as treatment with
steroids can often be fatal. Several studies have advocated
urgent exploration in addition to intensive support and
medical management when the diagnosis has been made.
Aristizabal et al reviewed their experience of 50 adult
patients with fulminating amebic colitis over an 18-year
period and reported a mortality rate of 60% for the
various operative procedures performed.30 Additional
studies in the literature support a mortality rate of 50%
to 100% (Table 1).1,3038 Finally, fulminating colitis has
been observed with increasing frequency in patients
suffering from malnutrition, diabetes, and other chronic
The classic operative nding in a patient with
fulminating colitis is an inamed, extremely friable
colon. It is wrapped with omentum, which conceals
the underlying full-thickness necrosis and perforation.
The colon is so friable that it can disintegrate with any
form of manipulation.31 The mucosal lining is often
replaced by necrotic debris with the lumen being lled
with foul-smelling pus.

Table 1 Mortality Rates of Necrotizing Amoebic Colitis:

Review of the Literature

Chen et al
Vajrabukka et al31


Elhence et al32

Mortality (%)



Wig et al34


Giacchino et al35


Stein et al36




Hadley and Mickel38



Ellyson et al1
Aristizabal et al30



Table adapted from Ellyson et al.1


Resection of the necrotic colon is the treatment of

choice.30,32 However, the extent of resection depends on
the degree of colonic involvement. If only the right colon
is involved, a right colectomy with an ileostomy and
mucous stula is the preferred management strategy.
Frequently, the entire colon is involved, and these
patients often require a total abdominal colectomy.
Primary anastomosis is never an option as these patients
are often critically ill and there is a high risk for suture
line dehiscence. Other forms of management include
diverting the fecal stream with a loop ileostomy and
blow-hole colostomy,39 simple suture repair of the
perforations and drainage, and exteriorization of the
diseased segment. These procedures are fraught with
signicant complications, perhaps because they leave the
diseased colon behind. Luveno reported experience with
45 patients with transmural amebic colitis treated with
intraoperative prograde colonic lavage and diverting loop
ileostomy.40 This is based on the previous observation
that the adhesive wraps help seal perforations and have
the capacity to revascularize the ischemic colon.6 Disturbing these wraps could have a deleterious effect. The
reported mortality was 13% after the initial phase of
the procedure and 5% after ileostomy closure. Despite
the small numbers and lack of randomization, this study
represents an attractive alternative to a radical resection
with its associated high mortality rate.
Amebic Liver Abscesses
The management of amebic liver abscesses is distinctly
different from that of other forms of hepatic abscesses.
The majority of patients respond to metronidazole
therapy within 72 to 96 hours.28,29 These patients should
also be treated with a luminal agent to eliminate the
intestinal source. Surgical or percutaneous drainage of
uncomplicated abscesses is usually not necessary and
should generally be avoided. However, aspiration of
large abscesses (> 300 cm3) appears to decrease hospital
stay and improve overall clinical status.41 Aspiration
should be considered in individuals where the diagnosis
is in question (such as pyogenic liver abscesses), there is
failure of medical management, or there are large left
lobe abscesses (potential for rupture into the pericardium) and in severely ill patients where rupture may be
imminent.5 Certainly, aspiration or catheter drainage
has a role in amebic empyema and has demonstrated
improved outcomes. There may also be a role for
percutaneous techniques as well as surgical drainage in
patients with amebic pericarditis.42
Despite its low incidence within the United States,
amebiasis can be a source of signicant morbidity and
mortality if not recognized early. Most forms respond


appropriately to medical therapy. Surgery and other less

invasive techniques are reserved for nonresponders and
patients presenting in acute distress.
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